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热休克蛋白70对血管紧张素II诱导的血管平滑肌细胞肥大的抑制作用。

Inhibitory effect of Hsp70 on angiotensin II-induced vascular smooth muscle cell hypertrophy.

作者信息

Zheng Ying, Im Chang-Nim, Seo Jeong-Sun

机构信息

ILCHUN Molecular Medicine Institute, Seoul National University College of Medicine, Seoul 110-799, Korea.

出版信息

Exp Mol Med. 2006 Oct 31;38(5):509-18. doi: 10.1038/emm.2006.60.

Abstract

Angiotensin II (Ang II), which is an important mediator of both vascular responsiveness and growth, has been shown to induce vascular smooth muscle cell (VSMC) hypertrophy via the activation of a complex series of intracellular signaling events. Heat shock protein 70 (Hsp70) has recently been shown to protect against Ang II-induced hypertension. In this study, we tested the hypothesis that Hsp70 can protect VSMC from Ang II-induced hypertrophy. We treated VSMCs with Ang II to induce hypertrophy and to activate MAPK signaling pathway. We observed that the augmentation of Hsp70 expression inhibited Ang II-stimulated VSMC hypertrophy. This inhibitory effect of Hsp70 appears to be partly due to extracellular signal-regulated kinase (ERK1/2) inactivation, which in turn, may possibly result from the accumulation of MAP kinase phosphatase-1 (MKP-1).

摘要

血管紧张素II(Ang II)是血管反应性和生长的重要介质,已被证明可通过激活一系列复杂的细胞内信号事件来诱导血管平滑肌细胞(VSMC)肥大。热休克蛋白70(Hsp70)最近被证明可预防Ang II诱导的高血压。在本研究中,我们检验了Hsp70可以保护VSMC免受Ang II诱导的肥大的假说。我们用Ang II处理VSMC以诱导肥大并激活丝裂原活化蛋白激酶(MAPK)信号通路。我们观察到Hsp70表达的增加抑制了Ang II刺激的VSMC肥大。Hsp70的这种抑制作用似乎部分归因于细胞外信号调节激酶(ERK1/2)的失活,而这反过来可能是由丝裂原活化蛋白激酶磷酸酶-1(MKP-1)的积累所致。

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